Neuroprotective Activity of Eriodictyol Against Streptozotocin-Induced Diabetic Peripheral Neuropathy in Wistar Rats by Targeting Wnt/β-Catenin Pathway

Abstract

AbstractThe present study explored the bioactivity of eriodictyol (Ed) in streptozotocin (STZ) induced diabetic neuropathy (DPN) and the probable role of the Wnt/β-catenin pathway. STZ (55 mg/kg,i.p.) was given to Wistar rats to induce diabetes. Ed (1 or 10 mg/kg, oral) or gabapentin (Gpn) (50 mg/kg,i.p.) or methyl vanillate (MV) (100 mg/kg,p.o.) was administered for 4 weeks starting 6 weeks after STZ administration. Feed/water intake, body weight (b.w.), blood glucose, insulin, glycosylated hemoglobin (HbA1c), and neuropathic pain parameters were measured at different intervals. Biomarkers of oxidative stress and inflammation were determined in the sciatic nerve after 10 weeks. The data indicated that Ed or Gpn attenuated STZ-induced increase inb.w., polydipsia, polyphagia, glucose, insulin, and HbA1c levels. Ed or Gpn ameliorated oxidative stress and inflammatory biomarkers in the sciatic nerve of STZ-injected rats. The neuropathic pain parameters were significantly amended in Ed or Gpn-treated rats against DPN. MV (Wnt/β-catenin activator) significantly potentiated the neuropathic effects of STZ. However, Ed (10 mg/kg) ameliorated these indices and improved the pain parameters in STZ and MV-treated rats. It can be concluded that Ed ameliorated the pathogenic course of DPN and pain parameters possibly by antagonizing the Wnt/β-catenin pathway.